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PubMed1990

Chromosome damage in rat pulmonary alveolar macrophages following ozone inhalation.

To determine whether ozone is clastogenic at environmentally relevant exposure levels, rats were exposed for 6 h to 0.0, 0.12, 0.27, or 0.80 ppm ozone. The alveolar macrophages were isolated from animals sacrificed 28 h after the end of the exposure. The mitotic index and frequency of chromosome aberrations were determined. No change in the mitotic index was detected following 0.12 ppm ozone exposure. A significant decrease in mitotic index was observed after exposure to 0.27 ppm ozone; a significant (4-fold) increase in the frequency of dividing macrophages was detected following exposure to 0.8 ppm ozone. Only chromatid-type aberrations were observed. There was a significant increase in the frequency of cells with chromatid gaps and in the frequency of cells with chromatid deletions. Animals exposed to 0.27 ppm ozone had the highest proportion of cells with chromatid deletions (0.172) relative to background level (0.028). No exchanges or chromosome-type aberrations were detected in any of the animals. These data suggest that ozone, at relatively low levels, is clastogenic in macrophages from exposed rats.

Administration, Inhalation↗
PubMed1992

Age-dependence of responses to acute ozone exposure in rats.

Previous work from this laboratory demonstrated that neonatal rats and postweanling rabbits are more sensitive to ozone-induced stimulation of pulmonary arachidonic acid (AA) metabolism than are young adults (Fundam. Appl. Toxicol. 15, 779.) In the study reported here, we have extended our initial investigation to include the influence of animal age on temporal aspects of pulmonary AA metabolism and several other responses to brief exposures to 1 ppm ozone. Rats of discrete ages ranging from 13 days to 16 weeks were exposed to 1 ppm ozone or to air for 2, 4, or 6 hr. Immediately following exposure the lungs were lavaged with six consecutive volumes of phosphate-buffered saline and the acellular fluid from the first lavage volume recovered was analyzed for its content of prostaglandin E2 (PGE2), protein, and lactate dehydrogenase. Leukocytes recovered by lavage were quantitated and characterized by viability and percentage of polymorphonuclear (PMN) cells. Several lines of evidence verified that PGE2 was produced by the lung as a consequence of ozone exposure and that its concentration in the fluid from the first lavage was a reasonably good index of pulmonary AA metabolism to prostanoids. We also demonstrated that the lavage process itself stimulates the lung, resulting in increased AA metabolism to prostanoids that were recovered in the second and following lavage volumes. The time course of PGE2 production by the ozone-exposed lung varied considerably with animal age. Neonatal rats 13 days of age were the most sensitive to ozone stimulation. At 2 hr of exposure, PGE2 concentration in the first lung lavage of these animals peaked at values approximately two orders of magnitude above controls and then decreased sharply with continued exposure. Adults and older neonates (18 days of age) were much less responsive to 2-hr exposures; however, continued exposure of these rats for up to 6 hr resulted in increasing PGE2 concentration in the first lung lavage. Other responses showed various degree of age dependence. The percentage of lavaged leukocytes that were nonviable (i.e., trypan blue-positive) showed a strong inverse correlation with animal age. In 13-day-old rats that were exposed for 6 hr, the percentage of dead leukocytes reached nearly 50%. In addition, sheets or clumps of dead cells that were judged to be epithelial cells were lavaged from these animals. Conversely, 16-week-old adult males exposed to ozone for 6 hr showed little evidence of damage to cells of the respiratory tract.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1986

Synergistic interaction of ozone and respirable aerosols on rat lungs. I. Importance of aerosol acidity.

A synergistic interaction, as defined by biochemical and morphological criteria, between ozone (or NO2) and respirable aerosols of ammonium sulfate or sulfuric acid has been described previously. Experiments in the present paper show that it is the acidity, not the sulfate content, of the aerosol that is responsible for such synergy; neutral aerosols of Na2SO4 or NaCl do not elicit synergistic effects when combined with ozone. Aerosol size (and, therefore, site of deposition in the lung) is also an important determinant of synergy with ozone; 0.5 micron mass median aerodynamic diameter (MMAD) aerosols are effective whereas 0.02 micron MMAD aerosols are not. The synergistic interaction between ozone and acidic aerosols could be demonstrated by biochemical and toxicological criteria in addition to those we have previously reported, for example increases in whole lung protein content and free (acid-soluble) proline content of lungs. A synergistic interaction has been demonstrated at concentrations of 0.64 ppm (1.3 mg/m3) of ozone and 1 mg/m3 of acid aerosol in this study. We conclude that acidity of an aerosol determines whether or not it interacts synergistically with ozone, and that an aerosol size that impacts maximally upon the alveolar duct region of the lung is most active with ozone.

Aerosols↗
PubMed1990

Effects of chronic exposure to ozone on pulmonary lipids in rats.

Ozone is the most toxic component of photochemical oxidant air pollution. Exposure to high concentrations of ozone produces a variety of toxic effects in the lung, but it is not known to what extent prolonged exposure to low concentrations of ozone may contribute to the development of chronic lung disease. Phospholipids, important components of cellular membranes and surfactant, are necessary for the maintenance of normal lung structure and function. In order to test the effects of chronic exposure to environmentally relevant concentrations of ozone on phospholipid metabolism in the lung, rats were exposed to clean air or to 0.12, 0.25 or 0.50 ppm ozone for up to 18 months. The content and biosynthesis of phospholipids in both lung tissue and bronchopulmonary lavage fluid (surfactant) were measured. Incorporation of [14C]acetate into lung tissue phospholipids, an estimate of overall biosynthesis, decreased significantly at some time points in the study, while tissue phospholipid content tended to increase with both ozone concentration and with age. No changes were detected in phospholipid content of bronchopulmonary lavage fluid. These findings did not support the hypothesis that prolonged exposure of rats to environmentally relevant concentrations of ozone results in either qualitative or quantitative deficits in the pulmonary surfactant system.

Animals↗
PubMed1991

Effects of ozone on cellular ATP levels in rat and mouse alveolar macrophages.

Hydrogen peroxide (H2O2) is thought to be a major intermediate in the toxicity of ozone. In a previous study we demonstrated that ATP depletion may play an important role in the H2O2-induced inhibition of the phagocytic functions of alveolar macrophages. Ozone exposure can adversely affect the phagocytic capacities of alveolar macrophages. In the present study we investigated whether a decrease in the cellular ATP concentration may underly the effects of ozone on alveolar macrophages. Neither following single (6 and 12 h) exposure nor repeated (12 h/day for 3 and 7 days) exposures of mice or rats to 0.4 ppm ozone, were decreased levels of ATP found in the alveolar macrophages. In contrast, repeated exposures of mice for 7 days to ozone led to a significant increase (1.5-fold) in the ATP content of the alveolar macrophages. In vitro ozone exposure of rat and mouse alveolar macrophages also did not lead to a decrease in the cellular ATP concentration. These results showed that ATP depletion does not play a role in the toxicity mechanism of ozone for alveolar macrophages.

Adenosine Triphosphate↗
PubMed1987

Quantitation of ozone-induced lung lesion density after treatment with an interferon inducer or an anti-interferon antibody.

Inhalation of ozone by experimental animals produces activation of lymphocytes in the mediastinal lymph node complex. Both the number and functional reactivity are affected, with evidence of blastic transformation in T cell but not B cell areas of the nodes. In the present work we determine the extent that modulation of a possible product of immune system activation, interferon, is capable of influencing the way that experimental animals respond to zone. Outbred CD-1 mice were treated with an interferon inducer, poly I:C, or with an anti-interferon antibody while being exposed to ozone at a concentration of 0.7 or 0.9 ppm for 20 h per day for 4 days. Interferon induction produced a significant reduction in lesion volumes in both exposure groups, while anti-interferon produced the opposite effect. Less alveolar damage was observed in interferon-induced, ozone-exposed animals than in animals exposed to ozone alone. In contrast, anti-interferon-treated, ozone-exposed animals showed larger lesions which extended to more peripheral structures and were more extensively infiltrated with neutrophilic leukocytes. These results show that interferon induction protects against zone-mediated lung damage. They also suggest that cells are activated during ozone inhalation which mitigate the effects of ozone on the lung by secretion of interferon.

Animals↗
PubMed1994

The effects of ozone exposure on lactate dehydrogenase release from human and primate respiratory epithelial cells.

Ozone is the most persistent, wide-spread air pollutant in the United States. Over one half of the population of the US lives in cities or suburban areas which do not meet the National Ambient Air Quality Standard for ozone which is 0.12 ppm averaged over 1 h. Controlled laboratory exposures of human subjects have shown that ozone exposure produces decreased pulmonary function, hyperresponsiveness to inhaled methacholine, inspiratory pain, and airway inflammation as assessed by bronchoalveolar lavage. However, the cellular mechanisms responsible for such effects are incompletely known. The present study examined the effects of ozone exposure at 0.50 ppm for 3 h on three types of cultured respiratory epithelial cells; primary cultures of human nasal cells and primate bronchial cells, and the A549 type II pneumocyte-derived cell line. Cells were grown to confluent monolayers in plastic 6-well plates and then exposed to ozone or filtered air on a tilting platform over a heated water bath. Lactose dehydrogenase release was significantly increased following ozone exposure of all cell types; a 75% increase from human nasal cells (P = 0.0002), a 79% increase from primate bronchial cells (P = 0.003), and a 69% increase from A549 cells (P = 0.02). These data suggest that even brief ozone exposure causes membrane injury to cultured human respiratory epithelial cells.

Adolescent↗
PubMed1994

Destruction of human tear proteins by ozone.

By an in vitro system human tears from healthy donors were exposed in a sealed vessel to a single dose of ozone. A marked destruction of tear proteins by ozone was observed as indicated by the disappearance of the protein pattern in polyacrylamide gel electrophoresis compared with the control. Lysozyme, a significant protein in tears, was demonstrated to be susceptible to degradation by O3. The destruction of tear proteins by ozone can be determined quantitatively by radial immunodiffusion as shown for human tear albumin. Variations of ozone concentrations and reaction time showed that destruction of tear proteins by ozone depended on the ozone concentration and occurred within a few minutes of exposure of tears to ozone.

Adult↗
PubMed1990

A study of ozone-induced edema in the isolated rat lung in relation to arachidonic acid metabolism, mixed-function oxidases and angiotensin converting enzyme activities.

In order to elucidate the role of arachidonic acid in the pathogenesis of ozone-induced pulmonary edema, isolated rat lungs were exposed to 14C-arachidonic acid in the presence or absence of ozone and the incorporation of radiolabelled arachidonate into pulmonary cell lipids was studied. The perfusates from these studies were also subjected to differential extraction and thin layer chromatography (t.l.c.) to determine synthesis of both cyclo-oxygenase and lipoxygenase products. In the presence of an edemagenic concentration of ozone, isolated lungs incorporated significantly less exogenous arachidonic acid into phosphatidyl choline and phosphatidyl ethanolamine, whereas incorporation into phosphatidyl inositol or serine was not affected. The edemagenic concentration of ozone also increased production of a variety of arachidonic acid metabolites via cyclo-oxygenase and lipoxygenase pathways. In separate studies, a similar ozone exposure did not affect 14CO2 production, resulting from the metabolism of 14C-antipyrine by mixed function oxidases (MFO). Similarly, an edemagenic concentration of ozone did not affect pulmonary angiotensin converting enzyme activity (ACE) as determined by the rate of formation of 14C-hippuric acid from 14C-hippuryl-histidyl-leucine (14C-HHL). Thus, acute ozone exposure is specifically associated with a reduced incorporation of arachidonate into phospholipids and with an increased conversion of arachidonate into bio-active metabolites.

Animals↗
PubMedDate not supplied

Ozone therapy effects on biomarkers and lung function in asthma.

BACKGROUND: The relationship and behavior of serum immunoglobulin E (IgE) level, peripheral blood mononuclear cell (PBMC) human leukocyte antigen DR (HLA-DR) expression and erythrocyte glutathione antioxidant pathway in asthma patients treated with systemic ozone therapy have not been studied before. METHODS: Asthma patients were treated about 1 year with three cycles (5 or 6 months each) with three different ozone therapy protocols. Ozone major autohemotherapy (MAHT) was applied at doses of 4 and 8 mg, 15 sessions each cycle; and ozone rectal insufflations (RI) at a dose of 10 mg, 20 sessions each cycle. Serum IgE, HLA-DR expression in PBMC and biomarkers for antioxidant pathway were measured before and at the end of each cycle. Lung function and symptoms test were recorded at the beginning and after the third cycle. RESULTS: IgE and HLA-DR decreased with the three types of treatments, while increments in reduced glutathione, glutathione peroxidase, glutation reductase and glutathione S-transferase were achieved with all treatments. Lung function and symptoms test were markedly improved. However, in all parameters the best response was obtained in the order: MAHT at 8 mg better than MAHT at 4 mg better than RI at 10 mg. Before ozone treatment, glutathione antioxidant parameters were under the normal reference values, suggesting the occurrence of oxidative stress associated with atopic asthma. CONCLUSIONS: This study demonstrates the effectiveness of ozone therapy in reducing IgE and inflammatory mediators along with the induction of antioxidant elements. The study raises the role of systemic ozone therapy in atopic asthma by means of its immunomodulatory and oxidative stress regulation properties.

Adolescent↗
PubMed2004

The enhancement of the biodegradability of phenolic solution using preozonation based on high ozone utilization.

In this research, the effects of preozonation on the biodegradability of 4-cresol, 4-nitrophenol and 2-chlorophenol solutions were investigated using a new gas-inducing reactor with high ozone utilization rate. The extent of preozonation may be monitored by determining the characteristic ozonation behaviors of preozonized phenolic solutions, such as residual phenolic concentration, ADMI value and ozone gas outlet concentration. Experimental results showed that as the initial phenolic compounds decomposed completely, the ozone gas outlet concentration rapidly increases. In addition, at pH 7, a peak ADMI value appears during the preozonation of 4-cresol and 2-chlorophenol, while for 4-nitrophenol the ADMI value decreases monotonically. Based on the characteristic ozonation behaviors and the ozone utilization rate, three characteristic times were chosen in order to have better control on the extent of preozonation. The effect of preozonation on the biodegradability of preozonized phenolic solution was studied based on these characteristic times. The intermediate products during the preozonation were also identified. The variation of BOD5 is strongly dependent on the accumulation of intermediate products. It is suggested that the best characteristic time is as the rapid increase of ozone gas outlet concentration in this study. The biodegradability (BOD5/COD) of preozonized 4-cresol, 2-chlorophenol and 4-nitrophenol solutions increase to 0.18, 0.26 and 0.33, respectively, for the best characteristic time.

Biodegradation, Environmental↗
PubMed2004

Fate of biodegradable dissolved organic carbon produced by ozonation on biological activated carbon.

The adsorption and desorption characteristics of BDOC produced by ozonation and the replacement of BDOC by non-BDOC on BAC was studied. The fate of BDOC produced by ozonation in the BAC column was also evaluated by comparative experiment between the BAC supplied with the mixture of BDOC and non-BDOC and the BAC supplied only with non-BDOC. Fulvic acids extracted from two river sediments and one forest soil were used. BDOC produced by ozonation showed the same or lower adsorption capacity than non-BDOC after biodegradation. The adsorption rate of BDOC on GAC was lower than that of non-BDOC. BDOC produced by ozonation had low desorbability and majority of BDOC produced were not replaced by non-BDOC. BDOC in the ozonated fulvic acid did not affect the breakthrough of the ozonated fulvic acid on GAC in the early stage of adsorption, suggesting that most of BDOC were biodegraded on the surface of GAC before adsorption. Therefore, the production of BDOC by ozonation before the GAC treatment is very effective for the extension of GAC service life and the reduction of DOC loading to GAC.

Adsorption↗
PubMed2005

Therapeutic efficacy of ozone in patients with diabetic foot.

Oxidative stress is suggested to have an important role in the development of complications in diabetes. Because ozone therapy can activate the antioxidant system, influencing the level of glycemia and some markers of endothelial cell damage, the aim of this study was to investigate the therapeutic efficacy of ozone in the treatment of patients with type 2 diabetes and diabetic feet and to compare ozone with antibiotic therapy. A randomized controlled clinical trial was performed with 101 patients divided into two groups: one (n = 52) treated with ozone (local and rectal insufflation of the gas) and the other (n = 49) treated with topical and systemic antibiotics. The efficacy of the treatments was evaluated by comparing the glycemic index, the area and perimeter of the lesions and biochemical markers of oxidative stress and endothelial damage in both groups after 20 days of treatment. Ozone treatment improved glycemic control, prevented oxidative stress, normalized levels of organic peroxides, and activated superoxide dismutase. The pharmacodynamic effect of ozone in the treatment of patients with neuroinfectious diabetic foot can be ascribed to the possibility of it being a superoxide scavenger. Superoxide is considered a link between the four metabolic routes associated with diabetes pathology and its complications. Furthermore, the healing of the lesions improved, resulting in fewer amputations than in control group. There were no side effects. These results show that medical ozone treatment could be an alternative therapy in the treatment of diabetes and its complications.

Adult↗
PubMed2004

A cumulative ozone uptake-response relationship for the growth of Norway spruce saplings.

Norway spruce saplings [Picea abies (L.) Karst.] were exposed during four growing seasons to different ozone treatments in open-top chambers: charcoal filtered air (CF), non-filtered air (NF) and non-filtered air with extra ozone (NF+, 1.4xambient concentrations). The CF and NF+ ozone treatments were combined with phosphorous deficiency and drought stress treatments. The total biomass of the trees was harvested at different intervals during the experimental period. The ozone uptake to current-year needles of the Norway spruce saplings was estimated using a multiplicative stomatal conductance simulation model. There was a highly significant correlation between the reduction of total biomass and the estimated cumulative ozone uptake, which did not vary when different thresholds were applied for the rate of ozone uptake. The reduction of the total biomass was estimated to 1% per 10 mmol m(-2) cumulated ozone uptake, on a projected needle area basis.

Air Pollutants↗
PubMed2004

Does interspecific competition alter effects of early season ozone exposure on plants from wet grasslands? Results of a three-year experiment in open-top chambers.

Chronic effects of ozone on wet grassland species early in the growing season might be altered by interspecific competition. Individual plants of Holcus lanatus, Lychnis flos-cuculi, Molinia caerulea and Plantago lanceolata were grown in monocultures and in mixed cultures with Agrostis capillaris. Mesocosms were exposed to charcoal-filtered air plus 25 nl l(-1) ozone (CF+25), non-filtered air (NF), non-filtered air plus 25 nl l(-1) ozone (NF+25) and non-filtered air plus 50 nl l(-1) ozone (NF+50) early in the growing seasons of 2000 through 2002. Ozone-enhanced senescence and visible foliar injury were recorded on some of the target plants in the first year only. Ozone effects on biomass production were minimal and plant response to ozone did not differ between monocultures and mixed cultures. After three years, above-ground biomass of the plants in mixed culture compared to monocultures was three times greater for H. lanatus and two to four times smaller for the other species.

Air Pollutants↗
PubMed2004

Ozone exposure triggers the emission of herbivore-induced plant volatiles, but does not disturb tritrophic signalling.

We evaluated the similarities between ozone-induced and mite-induced emission of volatile organic compounds (VOCs) from lima beans, and tested the response of the natural enemies of herbivores to these emissions using trophic system of two-spotted spider mites and predatory mites. The acute ozone-exposure and spider mite-infestation induced the emission of two homoterpenes, (E)-4,8-dimethyl-1,3,7-nonatriene and (E,E)-4,8,12-trimethyl-1,3,7,11-tridecatetraene, and (Z)-3-hexenyl acetate. Only plants with spider mite-infestation emitted the monoterpene (E)-beta-ocimene. Predatory mites were equally attracted to ozone-exposed and unexposed plants, but discriminated between spider mite-infested and uninfested plants, when both were exposed to ozone. The similarities between ozone and herbivore-induced VOCs suggest that plant defence against phytotoxic ozone and the production of VOCs for attraction of the natural enemies of herbivores may have adaptive coevolution. However, the expected elevated ozone concentrations in future may not disturb tritrophic signalling, unless herbivore-induced VOCs are lost in the process of aerosol formation.

Air Pollutants↗
PubMed2004

Sub-canopy deposition of ozone in a stand of cutleaf coneflower.

Although there has been a great deal of research on ozone, interest in exposure of native, herbaceous species is relatively recent and it is still not clear what role the pollutant has in their ecological fitness. The ozone exposure of a plant is usually expressed in terms of the concentration above the canopy or as a time-weighted index. However, to understand the physiological effects of ozone it is necessary to quantify the ozone flux to individual leaves as they develop, which requires knowing the deposition velocity and concentration of the pollutant as a function of height throughout the plant canopy. We used a high-order closure model of sub-canopy turbulence to estimate ozone profiles in stands of cutleaf coneflower (Rudbeckia laciniata L.) located in the Great Smoky Mountains National Park, USA. The model was run for periods coinciding with a short field study, during which we measured vertical concentration profiles of ozone along with measurements of atmospheric turbulence and other meteorological and plant variables. Predictions of ozone profiles by the model are compared with observations throughout the canopy.

Air Pollutants↗
PubMed2006

The effects of tropospheric ozone on the species dynamics of calcareous grassland.

Although ozone has been shown to reduce the growth of individual species and to alter the composition of simple species mixtures, there is little understanding of its long-term effects on species dynamics and composition in real communities. Intact turfs of calcareous grassland were exposed to four different ozone regimes in open-top chambers over three consecutive summers. Treatments provided a mean seasonal AOT40 ranging from approximately zero to 15 ppm h. Cumulative ozone exposure was a significant factor in compositional change, but only explained 4.6% of the variation. The dominant grass species (Festuca rubra) showed a consistent decline in cover in the high ozone treatment over time and the forb Campanula rotundifolia was lost from all three ozone treatments. The frequency of some species (Galium verum and Plantago lanceolata) increased with ozone exposure. Long-term effects of ozone on species composition in chalk grassland may be a function of both the sensitivity of individual species and the response of the dominant species.

Air Pollutants↗